"Sugar is the 2,000-pound gorilla" says Dr. Robert Lustig. The renowned expert reveals how ultra-processed foods drive chronic disease by causing mitochondrial dysfunction. Want better health? Reducing sugar might be more effective than expensive medications. #NutritionFacts
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Speaker 1 (00:03):
What is the largest restaurant chain in the US?
Speaker 2 (00:07):
It is our nation's public schools.
They're three times bigger thanSubway, mcdonald's, burger King
and Wendy's all combined.
It's triple the size.
And our kids are getting sickerand sicker.
Speaker 1 (00:19):
Hello friends, old and new, and welcome to Drinks
with Caroline.
I'm so happy you've joined mefor what I believe will be
another stimulating conversationwith an industry expert,
founder or otherwise fabulousperson in the consumer industry.
Dr Robert Lustig, welcome toDrinks with Caroline.
(00:40):
I'm so excited to be asking youquestions 11 years or so later,
given that I got the wonderfuljob of doing this at the Hong
Kong Forum when I worked forCLSA, and then we had a dinner
afterwards and I was just blownaway by all the facts that you
gave us about the impact ofsugar on our metabolisms.
And I'm no less blown away inlistening to Dr Andrew Huberman
(01:06):
and you discussing this towardsthe end of last year, and so I'm
just very grateful that you'veagreed to come onto my podcast
Drinks with Caroline.
We are now supposed to splitopen a drink.
Speaker 2 (01:16):
Well, I'm just going to ask you would you rather it
be a sparkling water, or wouldyou rather it be a scotch?
You choose.
Speaker 1 (01:22):
Well, I must admit, given it's still morning in LA,
I am drinking a coffee right now.
Well, how do you start your day, Robert?
Speaker 2 (01:29):
Black coffee only.
Speaker 1 (01:31):
Black only.
Well, I've got to wean myselfoff oat milk, but unfortunately
it has sugar in it and I'maddicted, so I think this is a
great starting point.
Dr Robert Lustig is an MD, aneuroendocrinologist, emeritus
professor of pediatrics at UCSFand a best-selling author, and
has appeared on many podcastsand other public forums to
(01:54):
discuss the impact of sugar onthe American diet.
I just have to say thateverything you've done the hard
work and heavy lifting overdecades now to try and raise
awareness that protein and fataren't bad and sugar is really
causing mitochondrial diseaseand all sorts of other issues
I'm in awe and I know that thattakes a lot of courage.
Speaker 2 (02:14):
The food industry.
Initially, for the first, Iwould say 15 years of my
advocacy had painted a target onmy back and did its ultimate to
discredit me and the notion.
And I think the reason isbecause sugar was their gravy
train.
Sugar is what brought them tothe feeding trough.
Sugar was what made the profitmargin of virtually every CPG
(02:37):
company go from 1% per year upto 5% per year.
And the reason is because sugaris addictive.
They did not want us to talkabout sugar being a
mitochondrial toxin, but thefact of the matter is it is.
The data has shown it andpeople are starting to
understand and incorporate thatconcept into their thinking.
Speaker 1 (02:57):
Could you just tell us a little bit about your
background in working withchildren and then your
observations that led you towhere you are today?
Speaker 2 (03:04):
Before I get started on that, I want to make one
thing clear to your audience,and that is it's not just sugar,
it's ultra-processed food.
In general, sugar is the2,000-pound gorilla, but there
are other issues withultra-processed food as well,
including the lack of fiber, thelack of omega-3s and also the
presence of emulsifiers.
(03:25):
All of these ultimatelycontribute to defective
metabolism and increasedinflammation, which are driving
all the chronic diseases that weknow of today.
Having said that, the easy one,the thing that's, you know,
sort of staring us in the facethat needs to be fixed and we
(03:45):
could fix it tomorrow if we hadthe political will is get rid of
the sugar.
So that's kind of where I startand where I finish.
That's kind of the alpha andthe omega of the story.
So how do I get started?
Look, I'm a pediatricneuroendocrinologist.
I'm interested in how the braincontrols hormones and how
hormones control the brain.
So I'm very interested inbehavior.
(04:08):
Well, obesity was kind of likethe final frontier of
endocrinology.
We didn't really understandobesity until we discovered this
hormone that goes from your fatcell to your brain, called
leptin.
So leptin was discovered in1994, so 30 years ago, and I was
, you know, right there, youknow well placed.
(04:31):
At the time of its discovery.
I actually worked atRockefeller University, which is
where leptin was discovered,and sort of knew all of the
protagonists in the leptindiscovery story, and so I was
very prepared and ready for itbecause I knew it was coming.
I had just moved to St JudeChildren's Research Hospital in
Memphis, tennessee.
So this is a pediatric cancerhospital, and at St Jude they
(04:55):
had a cadre of about 40 childrenwho had survived their brain
tumors only to become massivelyobese afterward, either due to
the tumor itself or the surgeryor the radiation.
So this form of obesity is wellknown in the literature.
It's been known since 1901.
It's called hypothalamicobesity because the hypothalamus
(05:18):
is the brain area that controlsenergy balance.
And clearly these children havea problem with their
hypothalamus and that's why theybecome obese.
And I now have 40 of them.
And what am I going to do forthem when they weigh 350 to 400
pounds?
What can I possibly help themwith?
(05:40):
Previously these kids had beenstudied by other investigators,
like, for instance, george Bray,who's the father of obesity
research in America, and headmitted eight of these with.
Previously these kids had beenstudied by other investigators,
like, for instance, george Bray,who's the father of obesity
research in America, and headmitted eight of these kids to
his research unit at Harbor UCLAMedical Center back in 1975.
And he locked them up and threwaway the key and he fed them
(06:00):
500 calories a day for a month.
What do you think their weightdid on 500 calories a day?
Plunged, it went up.
Wow, the kids are on starvationdiets and they're gaining weight
on starvation diets.
Are they breathing the caloriesin?
No, turns out, because of thehypothalamic damage.
(06:21):
Their brain thinks they'restarving and the reason is
because they can't see thishormone called leptin, because
those neurons are dead.
And when you can't see yourleptin, your brain thinks you're
starving.
And so what they did was theywent into energy conservation
mode, their sympathetic nervoussystem, which normally burns
(06:42):
energy, even at rest, even whileyou're sleeping, you still have
.
Even at rest, even while you'resleeping, you still have a body
temperature.
Even while you're sleeping,because your muscles are still
working, they're still turningover ATP.
Even while you're sleeping,even though you're not moving,
well, their temperatures are waylower because they're actually
trying to conserve energy.
So, even on 500 calories a day,they're still gaining weight
(07:05):
and, of course, they're hungrylike crazy.
And so I've got these kids, andwhat am I going to do for them?
So I knew from my endocrinetraining that there was a nerve
that led from the hypothalamusto the pancreas called the
dorsal motor nucleus of thevagus nerve.
People know about the vagusnerve called the dorsal motor
nucleus of the vagus nerve.
(07:26):
When people know about thevagus nerve, it's what gives you
butterflies in your stomach.
Maybe if we did something tosuppress their insulin release,
maybe they wouldn't gain theweight.
So there's a drug that'savailable that I knew about,
called octreotide, and normallyit's used to suppress growth
hormone, but it also suppressesinsulin, and so we decided to
(07:48):
repurpose it and see whether ornot we could help these kids.
And so we did a pilot trial witheight children with this very,
you know, worrisome disordercalled hypothalamic obesity.
And lo and behold, they startedlosing weight.
But something even moreremarkable occurred Not only did
they lose weight, they startedexercising spontaneously.
(08:09):
One kid became a competitiveswimmer.
Two kids started liftingweights at home.
One kid became the manager ofhis high school basketball team,
running around collecting allthe basketballs.
These are kids who sat on thecouch, ate Doritos and slept,
and now they're active and theparents are saying I've got my
kid back and the kid's sayingthis is the first time my head
hasn't been in the cloud sincethe tumor.
This is really remarkable.
The very first patient Itreated with octreotide, you
(08:31):
know, with this hypothalamicobesity.
I tell the mother look, I don'tknow what's going to happen.
This is your patient number one.
I need you to call me in oneweek and tell me what's going on
.
She calls me in five days,frantic screaming in the phone.
Speaker 1 (08:46):
Dr Lustig, something's happening.
Speaker 2 (08:49):
And I'm going.
Oh my God, oh my God, adverseevent, shut this study down, go
to jail.
I'm waiting for the other shoeto drop.
What happened?
What happened?
Well, normally we would go toTaco Bell and she would eat five
tacos and an encharito andshe'd still be hungry.
We just went to Taco Bell andshe ate two tacos and she was
(09:10):
full and she just vacuumed thehouse.
Wow, just vacuumed the house.
I mean, this was a kid who didnothing, okay, and she vacuumed
the house.
So something was going on.
And this was before she hadever had a chance to lose any
weight.
It was, you know, just fivedays.
Okay, this kid weighed 220pounds and she ended up losing
(09:33):
48 pounds on octreotype.
So this was very, veryinteresting.
And so we did the study again.
This time we did it as adouble-blind placebo control
trial, and it worked again.
And then we did the study again.
This time we did it as adouble-blind placebo-controlled
trial, and it worked again.
And then we asked the questioncould this be going on in normal
people that don't have braintumors, you know, obese people
(09:55):
without a lesion in theirhypothalamus?
About 20% of the normal obesepopulation of adults responded
to octreotide the same way thekids did, with a suppression of
insulin and an increase inactivity.
So what we learned from thatexperiment is that the two
(10:18):
behaviors that we associate withobesity gluttony and sloth are
actually mediated by thebiochemical changes coming from
the brain, that the behavior isactually due to the biochemistry
.
And this changed how Iapproached all of obesity and
really what got me on the map interms of obesity research.
Speaker 1 (10:41):
That's a real breakthrough and I can't even
imagine how exciting and, at thetime, mind blowing.
I think more and more people,and particularly younger people
and people who listen to theHuberman podcast there's a group
that absolutely buys this.
I wanted to ask you a littlebit about calories in and
calories out, the CICA, andthere is definitely a group of
(11:06):
people that still firmlybelieves it's how many calories
you consume.
Can we address that?
Speaker 2 (11:11):
All I can say is that calories in, calories out is a
belief system, because you can'treally determine whether the
calories are going in or goingout.
You don't know.
Okay, how are you going tofigure that out?
Speaker 1 (11:23):
Well, what about these aura rings and things that
measure the output?
Speaker 2 (11:27):
That doesn't tell you here's the issue.
The whole world thinks a calorieis a calorie.
Now, for your audience, what'sa calorie?
So a calorie is a unit of heat,it's a unit of physics.
It is how much energy does ittake to raise one gram of water?
One degree centigrade, that'swhat a calorie is.
Now, in 1902, wilbur Atwaterfigured out that fat had nine
(11:53):
calories per gram of fat andprotein had four calories per
gram of protein and carbohydratehad four calories per gram of
carbohydrate.
Therefore, fat was more energydense.
Therefore, fat is fattening.
Speaker 1 (12:11):
Oh, wow.
Speaker 2 (12:14):
Because if a calorie is a calorie, then that would be
true, that would work, exceptthat that's ignoring several
issues.
Number one except that that'signoring several issues.
Number one insulin is thedriver of weight gain, and we
know that because all you haveto do is look at a type one
diabetic and look how muchweight they lose, and then you
put them on insulin and look atall the weight they gain back.
(12:35):
Number one.
Number two we are not bombcalorimeters.
Okay, if you put, you know, fatin a bomb calorimeter, you get
nine calories per gram, but weare not bomb calorimeters.
Okay, if you put you know, fatin a bomb calorimeter, you get
nine calories per gram, but weare not bomb calorimeters.
We have these things in ourcells called mitochondria, and
mitochondria are not bombcalorimeters.
Mitochondria can bedysfunctional.
(12:58):
Mitochondria don't necessarilyturn energy into heat, they turn
it into ATP, and there arerules governing how that gets
manufactured.
So I'll give you four, you know, killers to the idea that a
(13:19):
calorie is a calorie.
Okay, let's start with fiber.
Okay, fiber.
You like almonds?
Speaker 1 (13:28):
I wish I did, I don't .
Speaker 2 (13:30):
Okay, well, I love almonds, so you just have to
deal with it.
Okay, you eat 160 calories inalmonds.
How many of those calories doyou absorb?
130.
You ate 160.
You absorbed 130.
Where'd the other 30 go?
(13:50):
They were chewed up by themicrobiome.
You didn't absorb them becausethe fiber in the almonds
prevented their absorption.
So, even though they passedyour lips, even though they
registered as a calorie eaten,if you didn't absorb it, you
didn't get it, and if yourmicrobiome did, your microbiome
might do something with that.
That might actually change yourbehavior, like generate short
(14:13):
chain fatty acids which mightactually be immunosuppressive
and anti-inflammatory and reduceyour food intake.
Speaker 1 (14:22):
Just a question on that.
Then If you drank almond milk,you would not see that happen,
because you wouldn't get thefiber.
Speaker 2 (14:28):
There's no fiber, right?
Almond milk has no fiber.
Basically, the fiber got thrownin the garbage.
Same thing when you juice afruit you throw the fiber in the
garbage.
Turns out the fiber is the goodpart of the fruit.
The juice is nature's way ofgetting you to eat your fiber.
Speaker 1 (14:45):
Robert, one of the things that stuck with me a
decade is when you explained thedifference between eating four
oranges and trying to drink thatmuch.
Well, sorry, drinking that muchorange juice was easy the juice
of four oranges.
Trying to eat four orangeswould make you feel sick.
Speaker 2 (15:07):
You will throw up Right.
Speaker 1 (15:09):
And that just demonstrated the fiber issue.
Speaker 2 (15:12):
Yes, exactly so.
If you only measured thecalories at your mouth, you
would think that there'ssomething wrong, but in fact if
you measure them at theintestine, then it makes much
more sense.
But then a calorie is not acalorie, because a calorie eaten
is not a calorie eaten becauseif it came with fiber, that
(15:33):
calorie wasn't for you, it wasfor your bacteria.
Problem number one.
Problem number two protein.
So protein, as you know, ismade up of amino acids and each
amino acid can be used as astructural building block to
create other proteins, or it canbe used for energy.
Now, as it turns out, if youuse an amino acid for energy,
(15:56):
the liver has to take the aminogroup off, so it becomes an
organic acid, and then thatorganic acid can be used for
energy.
Well, in order to take thatamino group off, it costs energy
.
You have to invest energy inorder to get energy out.
So the mean difference betweenwhat you can burn in a bomb
(16:21):
calorimeter versus what yourcells will do with it will be
different, because you had toinvest energy in your cells,
whereas you didn't have toinvest the energy in a bomb
calorimeter.
So a calorie is not a caloriebecause if it came from a
protein, it ain't going to addup.
Number three, fats.
(16:42):
So over here we have omega-3sheart healthy, anti-inflammatory
, anti-alzheimer's, save yourlife, single best thing you can
put in your body.
Over here we have trans fats,the devil incarnate, okay,
consumable poison.
They're both nine calories pergram.
One will save your life, onewill kill you, because a calorie
(17:03):
is not a calorie.
And finally, the big kahunafructose and glucose.
So glucose is the energy oflife.
Every cell on the planet burnsglucose for energy.
Glucose is so important that ifyou don't consume it, your body
makes it.
Fructose, on the other hand, iscompletely vestigial to all
(17:24):
human life.
There is absolutely nobiochemical reaction in any
vertebrate on this planet thatrequires fructose.
It is a holdover from our plantancestors.
When we split off, they wentwith fructose, we went with
glucose, and that's why they'replants and we're not the point
(17:44):
is that's a great line.
Okay, well, actually some humansare plants, let's be honest,
but no plant is a human.
The point is, fructose ismetabolized in the liver
completely differently frombeta-glucose.
And what fructose does is itdrives liver fat because it
poisons mitochondriaspecifically to generate the fat
(18:07):
.
And the reason is becausefructose was only available one
month a year.
It was called harvest time, andwhat came after harvest time?
Winter.
So the goal of harvest was tosnarf up all of this fructose as
much as you could and get itturned into fat so that you
could basically survive thewinter.
(18:29):
We call this phenomenon seasonalinsulin resistance, and
fructose is specifically amitochondrial toxin so that your
cells will turn away fromburning it to energy, to ATP,
and turn it toward generatingfat.
And that worked for us forhundreds of thousands of years
(18:53):
as an adaptive evolutionarymechanism.
But when fructose is available24-7, 365, like it is now, we
don't need that, but we've stillgot it and we're still turning
it into fat, and so it's liningour arteries, it's lining our
livers, it's causing insulinresistance and it's driving
chronic metabolic diseasebecause it is metabolized
(19:17):
differently from that of glucose, because a calorie is not a
calorie.
So in a bomb calorimeter, sure,but we are not bomb
calorimeters, and anybody whosays a calorie is a calorie is
obviously not listening and, tobe honest with you, that's most
people.
Speaker 1 (19:34):
So can we talk about addiction?
And you make a reallyinteresting point about the huge
, the tectonic shifts in theworld systems, particularly in
the US, I guess, over the last50 years or so.
And how do you think sugarcould play out?
Speaker 2 (19:51):
So the question is is sugar addictive?
Now let's look at alcohol,because alcohol and sugar are
very similar to each other.
Because, after all, where doyou get alcohol from
Fermentation of sugar?
They actually are metabolicallyequivalent and in the brain
they're equivalent as well.
40% of Americans areteetotalers never touch the
stuff.
40% are social drinkers.
(20:12):
Can pick up a beer, put it down, I'm in there.
10% are binge drinkers and 10%are chronic alcoholics.
So 20% of America have analcohol problem.
Now, what constitutes being analcoholic?
What constitutes being alcoholaddicted?
We don't know To this day.
We don't know.
(20:32):
We've been looking for thegenetics of alcoholism, haven't
found it.
We've been looking for thegenetics of smoking haven't
found it.
We don't know what leads oneperson to be addicted and
another person to not be.
But clearly some are and somearen't.
Well, the same thing for sugar.
Not everybody is addicted, butthose that are are.
(20:56):
And it's very easy to figureout who's who, because the
sugar-addicted person will tellyou oh, I have a horrible sweet
tooth.
That's sugar addiction, untilproven otherwise.
And the reason they'll tell youis because right now, that's
socially acceptable.
If, all of a sudden, sugaraddiction was not socially
acceptable, they wouldn't tellyou that, just like they won't
(21:17):
tell you they're an alcoholicand nowadays they won't even
tell you they're a smoker,because it's not socially
acceptable.
So I figure 20 to 25% ofAmerica is sugar addicted.
Okay, everyone likes it, butnot everyone needs it.
It's when you need it that'sthe problem.
(21:37):
Now, how do you know that it'saddictive?
Well, because it activates thesame reward mechanism as cocaine
, heroin, nicotine, alcohol,sugar, and it does the exact
same things.
And you can measure it in thebrain.
You can see it in the brain,you can measure it biochemically
, you can measure it with fMRI,you can measure it with PET
scanning.
It's doing the same thing andmore and more for less and less.
(22:03):
In other words, as the sugardose goes up, you end up with
less and less reward, the law ofdiminishing returns, also known
as tolerance, which is one halfof addiction.
The other half is eitherwithdrawal or dependence, and
sugar shows that as well.
So the bottom line is sugarmeets all the criteria for
(22:27):
addiction that cocaine, heroin,nicotine and alcohol do.
There's going to be a specialissue of the Frontiers in
Psychiatry all on food addictioncoming up later this year.
All about food addiction.
You know, when you actuallycome down to it.
There are only really two itemsin food that are truly
(22:50):
addictive, and they are sugarand caffeine.
Speaker 1 (22:54):
Is that why I'm enjoying my iced latte so much?
Speaker 2 (22:57):
You said it, I didn't .
Speaker 1 (22:58):
I'm going to be wearing a glucose monitor soon,
dr Lustig, and I'm wonderingwhat is going to happen when I
put that on and then drink this.
Speaker 2 (23:06):
You'll find out and that will help you understand
what your food is doing to yourmetabolic health, and it might
alter your choices.
And if you do, that will onlybe good.
So I am an advisor to a companyhere in the United States
called Levels Health, and whatwe do is we try to help people
(23:31):
understand what food does totheir metabolic health.
One of the tools at ourdisposal is the use of
continuous glucose monitors,because the higher the glucose
goes, the more insulin is goingto be released.
The more insulin is going to bereleased, the more weight
you're going to gain and theless well you're going to feel.
Glucose is a proxy for insulinand insulin is the driver of
(23:54):
weight gain.
So we have data to show thatpeople who use continuous
glucose monitors gain lessweight and, in many cases, lose
weight, and they also feelbetter, in part because they're
not having the highs and thelows, because those highs and
the lows make you eitherirritable or they make you
sleepy.
Speaker 1 (24:13):
That makes so much sense.
You've also developed youtalked about I think someone
else developed the NOVA system.
Can you talk a little bit aboutthat?
Speaker 2 (24:21):
Sure, I did not develop the NOVA system.
My colleague, dr Carlos Montero, who is a public health
epidemiologist at the Universityof Sao Paulo in Brazil, he
developed the NOVA system.
So what the NOVA system does isit categorizes food.
Instead of based on itsnutritional value, it
(24:43):
categorizes food based on itsdegree of processing.
There are four classes in NOVA.
So the easiest way to explainthis is with an example.
Let's take an apple.
Nova class one would be anapple picked off a tree.
Nova class two would be appleslices de-stemmed, de-seeded,
maybe de-skinned.
Nova class three would be applesauce, macerated, cooked,
(25:04):
possibly with a preservativeadded, maybe with extra sugar,
maybe not.
Nova class four would be aMcDonald's apple pie.
Now the question is how muchNova class 1 apple is in that
Nova Class 4 McDonald's applepie?
And the answer is onlyMcDonald's knows for sure.
But the question is are all ofthese different types of Nova
(25:28):
Class foods the same?
If you believe a calorie is acalorie, it shouldn't matter
where the calories came from.
So it shouldn't matter wherethe calories came from.
So it shouldn't matter if yourcalories came from, you know,
carrots or cheesecake orCoca-Cola or kumquats, because
if a calorie is a calorie, thenthey should all be equal.
(25:48):
Well, it turns out when youlook and Carlos did this when
you look at all the disease inthe data sets from all over the
world in terms of what peopleare eating, all the disease is
in that NOVA class four group.
None of it is in NOVA class onethrough three.
Speaker 1 (26:07):
How is that being measured?
When you say all the disease?
Speaker 2 (26:10):
The incidence of hypertension, the incidence of
diabetes, the incidence ofcardiovascular disease, the
incidence of cancer, theincidence of dementia, the
incidence of fatty liver disease, et cetera.
All of these chronic metabolicdiseases that are basically
killing people all over theworld and basically draining
healthcare dollars from everysingle developed and developing
(26:32):
country all over the world.
$11 trillion deficit per yearfor the care and treatment of
chronic metabolic disease, whichis more than the US or globally
.
That's globally.
Speaker 1 (26:44):
It's insane.
Speaker 2 (26:45):
But it's more than what the food industry is making
.
So that's not sustainable.
There's more money going outthan is coming in.
That's unsustainable.
And all of them aremitochondrial diseases and none
of them have treatments and allof them are driven by that.
Nova Class 4 ultra-processedfood category.
Speaker 1 (27:05):
It's interesting you say none of them have treatments
, because I guess GLP-1 drugsare not a treatment.
But what is your view of them?
Speaker 2 (27:13):
Okay, so how much time do we have?
Carolyn, glp-1s are complicatedand I'm going to be very honest
with you, I don't know theright answer to them.
I know a lot about them becauseI'm an endocrinologist.
I was there when the firstGLP-1 started being used, called
Xenotide, back in 2006.
And I've known about GLP-1 as amolecule as recently as 1987.
(27:36):
Okay, so it's been around for awhile, but NovoNordisk and
Lilly have done very big thingswith it.
I wear three hats I wear theclinician hat, I wear the
scientist hat and I wear thepublic health policy wonk slash
advocate hat, and how I feelabout GLP-1s depends on which
(27:57):
hat I'm wearing.
So when I'm wearing myclinician hat, I'm glad they're
here because they work.
I'm not saying they don't work.
They do work 16% weight lossfor semaglutide, 20% weight loss
for terzepatide.
They work.
And if you have morbid obesityand nothing else works, these do
, and that's a big deal.
(28:18):
So I'm glad they're here.
So, from a clinician standpoint, I'm very positive about them.
It just so happens most of thepeople who are taking it are not
people who need it, like, youknow, people in Hollywood.
That's a different problem.
That's an access problem, not aclinical problem.
Now let me put my scientist haton.
Why do they work?
Well, they work in two ways.
(28:41):
They work in two places.
The first place they work is onthe brain, and they work on
that reward center we talkedabout before to actually reduce
reward, so that basically, sugarin particular is not as
interesting, and so you cut downyour consumption of sugar,
ultra-processed food, et cetera,and that is good.
(29:01):
Now we had a drug available tous 20 years ago out of France,
from Sanofi, and the drug wascalled Ramanubant.
It was the anti-marijuana drug,it was an endocannabinoid
antagonist, it was theanti-munchies drug and it got
approved for obesity in Europe.
(29:22):
Never got approved in America,but in Europe it got approved.
And within two months of itsapproval and people starting to
use it, there were 21 suicidesand the drug got immediately
pulled.
And what we learned from thatlittle foray is rewards what
gets you up in the morning, andif you shut reward off, there's
(29:44):
no reason to live.
Well, glp-1 shuts off reward,and so GLP-1 agonists are
associated with an increasedincidence of depression.
We've been looking for suicideas a telltale sign of a problem.
So it's still on the market,but there's no question that
there is an increased risk ofdepression with the use of
(30:04):
GLP-1s because of its effects onthe brain.
But remember I said there weretwo places it worked.
The second place is on the GItract, specifically on the
stomach, and what it does is itreduces the rate of gastric
emptying.
It basically makes your GItract move slower and so you
(30:26):
don't want to eat because youstill got stuff in your stomach.
Right, so it's mechanical.
But what that does is it causesthe side effects the nausea,
the vomiting, the pancreatitisand, most recently, the
gastroparesis.
Gastroparesis stomach turns tostone.
3.9% of people who use GLP-1analogs get gastroparesis and,
(30:53):
of course, package insertdoesn't even say it.
So this is actually a lawsuitgoing on right now against the
GLP-1 companies forgastroparesis.
Speaker 1 (31:03):
Is it reversible or it just stays once you have it?
Speaker 2 (31:06):
So a lot of patients who have taken it and get
gastroparesis.
They go off it and thegastroparesis doesn't get better
.
So there's a big issue that's alittle bit concerning, don't
you think?
Speaker 1 (31:17):
It's a little terrifying, I think.
Speaker 2 (31:19):
And number three when you look at the weight loss,
when you look at what's actuallybeing lost, turns out to be
equal amounts of fat and muscle.
Losing fat is the good part,but losing muscle is not.
Losing muscle is a bad thing.
Ask any little old lady whobreaks her hip whether she
wishes she had a little bit moremuscle.
Losing muscle is associatedwith increased mortality,
(31:41):
sarcopenia, so losing muscle isnot such a good thing.
So what else causes you to losefat and muscle in equal amounts
?
Starvation, and why do youthink it's working?
It's because you're starving.
Okay, is that the best way tolose weight?
Starvation?
I don't think so.
Okay, it's been shown you know50 ways from Sunday that that's
(32:02):
not the best way to do this.
Okay, and only one third ofpeople who take GLP-1 analogs
actually lose any weight.
They only tell you about theresponders.
They don't tell you about theintent to treat model and
responders.
They don't tell you about theintent to treat model.
And so many people get sideeffects that they stop taking it
.
Or because it's so expensive,they stop taking it and all the
weight comes back plus some.
(32:23):
So what that's telling you isit's not actually fixing the
problem, it's just band-aidingthe problem, because the weight
all comes rushing back as soonas you stop it.
Okay, let me put my third hat on, my public health advocate hat.
All right, these drugs do work.
I'm not saying they don't, theydo.
All right, 16% weight loss forsemaglutide.
(32:47):
20% weight loss for zepatide.
True, okay, if everyone inAmerica who qualified for an
analog got it, that would be$2.1 trillion to the healthcare
system.
But the healthcare system is$4.1 trillion in expenses, so
that would be a 50% surchargeover what we're paying now.
(33:09):
We're paying now.
How are we going to afford a50% increase?
That's crazy, unless, of course, trump really means we're going
to reduce drug costs.
Ha ha, if you believe that Igot a bridge to sell you.
Conversely, and this is theimportant part, if we just got
added sugar consumption in thiscountry down to USDA guidelines
(33:32):
of 12 teaspoons per day, howmany grams in a teaspoon?
Four, so 12 would be 48 to 50.
Speaker 1 (33:40):
That doesn't sound so punitive, that sounds very
doable.
Well, it's not.
Speaker 2 (33:43):
That's the point.
It's not.
We're consuming 94 grams, Imean.
So basically it'd be cutting itin half.
If we just cut our sugarconsumption in half, we would
lose 29% weight loss.
We'd have 29% weight loss, sowe'd have better weight loss,
and instead of spending 2.1trillion, we would save 3.0
trillion.
So that's a $5.1 trillion swingwith better weight loss and no
(34:09):
side effects.
So which one makes more senseto you?
Speaker 1 (34:13):
Yep, you make some really, really interesting
points.
Can we talk a little bit?
I've seen the number that youthrew out that 73% of what's
sold in grocery stores has sugarin it or hidden sugars.
You know, I think theavailability of healthier food
is something most of thepopulation really does want now,
(34:36):
and I think if sugar is hiddenit makes it really hard to make
good choices.
Speaker 2 (34:42):
Indeed, indeed, and there are 262 names for sugar,
and the food industry uses allof them on purpose, because that
way they can hide it in plainsight, and that's one of the
reasons our consumption is at 94grams per day.
So we need fundamental reformof the entire food system.
(35:05):
I completely agree with that.
The question is will RFK beable to enact that?
Speaker 1 (35:14):
Does he want to do that.
Speaker 2 (35:16):
Well, he says he does , We'll see.
But I'm actually quiteconcerned because his initial
moves in this space do notportend confidence.
Speaker 1 (35:30):
Do you mean around the dyes, or do you mean his
views on vaccines?
Speaker 2 (35:33):
Both.
I'm holding my breath andbiting my tongue and waiting,
but the things that I see so farare not exciting me.
Like, for instance, he wants toget rid of food dyes.
So do I.
We don't need them.
I totally agree.
On the other hand, instead ofasking Congress to ban them,
(35:58):
hand.
Instead of asking Congress toban them, okay.
Or instead of getting HHS toyou know, exert an
administrative order to removethem, okay.
He's basically said to the foodindustry please stop.
And they haven't.
So what good is that?
Speaker 1 (36:14):
Right, so I now live in LA.
There's a lot of innovation.
There are a lot of companiesthat do want to put good
products on the shelves, and isit possible to have processed
food that isn't bad for you?
Speaker 2 (36:27):
Yes, it is.
So here's the issue Ourultra-processed food is killing
us.
Our ultra-processed food isdecidedly unhealthy.
I completely agree with that.
The question is canultra-processed food be?
Speaker 1 (36:46):
made healthy?
Speaker 2 (36:47):
That's a different question.
I've been working for the lastfive years with a company in the
Middle East.
It's called Kuwaiti DanishDairy Company, add, and they are
like the Nestle of the MiddleEast and they make all sorts of
bad stuff.
They make flavored milks, theymake frozen yogurts, they make
ice cream, they makeconfectionery, they make
(37:09):
biscuits, they make tomato sauce.
Okay, like you know, problemstuff.
In 2020, the CEO of KDD came tome and said look, we know we
have a problem.
Kuwait has an 18% diabetes rateand an 80% obesity rate.
Speaker 1 (37:27):
Did you say 80% obesity rate?
Speaker 2 (37:29):
An obesity rate, oh my gosh.
And we don't want to be part ofthe problem, we want to be part
of the solution.
Can you help us turn KDD into ametabolically healthy company?
And so I don't take any moneyfor this.
But I convened a group ofscientific advisors and we
basically stemmed the stern topto bottom, took all the stuff
down to the studs, basicallyevaluated every aspect of KDD's
(37:53):
operation in terms ofingredients that they buy from
suppliers, processing techniquesand their products, okay, and
we sent them for biochemicalanalysis to actually determine
what's in the stuff.
And in doing so, we came upwith a set of precepts to
basically help KDD move theirproducts from unhealthy to
(38:15):
healthy.
And there are three preceptsthat determine whether or not a
given food is healthy.
And here are the three Protectthe liver, feed the gut, support
the brain.
Any food that does all three ishealthy, ultra-processed or not
.
Any food that does none of thethree is poison, ultra-processed
or not.
So, yes, ultra-processed foodin America right now satisfies
(38:38):
none of those three.
But could it?
Well, it would meanre-engineering ultra-processed
food.
Well, that's what we did withKDD, and so over the last two
years, kdd has pulled orre-engineered 10% of their
entire portfolio.
Re-engineered 10% of theirentire portfolio 18 items out of
(39:01):
180 items to become to bemetabolically healthy.
And then we've tested those inpeople to determine their
metabolic responses either theirglucose and insulin responses
or their GI responses, et ceterato determine whether or not
these maneuvers actuallyconferred health instead of harm
to these products.
And they are now on the marketin Kuwait.
(39:23):
So we wrote this up inFrontiers in Nutrition in 2023,
and we offered it to the worldas a roadmap for other companies
that want to do the same thing.
And what I can tell you is we'vehad no takers, and the answer
is because, number one, they'reafraid.
Number two, sugar's their gravytrain.
(39:44):
And number three, while theywould like to do something, they
have to worry about their wallstreet quarterly reports and
their stockholders.
In addition, if they said tothe public you know all that
processed food, we've been, youknow, serving up for the last,
you know 70 years, it's reallynot've been, you know, serving
up for the last, you know 70years.
It's really not that good foryou because we're going to try
to make it better.
Okay.
What they do is they losemarket share, they lose
(40:06):
reputation and they generatelawsuits.
This is all because they'reafraid.
Speaker 1 (40:11):
Demands of a shareholder group versus what
most human beings actually dowant to do and get right, I
think.
Speaker 2 (40:18):
Well, you know, the food industry is filled with
good people who want to do theright thing.
The problem is, they work for afood company.
Speaker 1 (40:25):
Can we talk about non-nutritional sugars like
replacements for sugar?
What is your view on those?
Speaker 2 (40:32):
If you believe a calorie is a calorie, then they
should be good because they'reno calories.
No fructose should be better.
Right Turns out, the metabolicdetriment of artificial
sweeteners does not go throughcalories or fructose, it goes
through other things.
So the toxicity of one sugarbeverage equals the toxicity of
(40:54):
two diet beverages.
Now you say to me, how can thatbe?
No sugar, no fructose, nocalories?
Well, it turns out those dietsweeteners do other things.
Number one they still generatean insulin response which still
generates weight gain.
And so it's been shown thatthrough meta-analyses that diet
sweetener consumption does notactually cause weight loss,
(41:18):
whereas if they did work theyshould cause weight loss, but
they actually don't because theystill generate an insulin
response.
And the second thing is thatseveral of the diet sweeteners
not all of them, but several ofthem actually cause GI
perturbations that lead tochanges in the microbiome,
glucose intolerance, leaky gutand therefore chronic
(41:39):
inflammation and systemicinsulin resistance, driving
chronic metabolic disease.
So even though these compoundsare zero calorie, that doesn't
mean they have zero effect.
Speaker 1 (41:53):
Which are the better diet sweeteners here.
Speaker 2 (41:56):
So we've done a full study of that for KDD and so I'm
very prepared to discuss it.
The one that seems to hold themost promise of all of them is
this compound called allulose,and allulose is an epimer of
fructose.
It seems to lower LDL and raiseHDL, which seems to be a good
thing from a cardiovascularstandpoint.
It seems to be able to be usedsimilar to sugar in terms of its
(42:20):
bulking capacity and itshumectant capacity and its
hardening capacity, so that'sgood.
It is 70% as sweet as sugar, soit can be used as a sugar
extender probably better as asugar extender than as a sugar
replacement, but even so seemsto have some benefit in value.
(42:41):
The problem with allulose rightnow is that it's 12 times as
expensive as sugar, so that'skind of keeping it out of the
market, and also the EuropeanFood and Safety Administration
has not approved it yet, in partbecause the way to make it is
with GMO processes, whichthey're not happy with.
So there are some questions.
And also now there are two newways of making allulose, so that
(43:04):
should reduce the pricesignificantly to maybe two times
the cost of sugar.
Speaker 1 (43:09):
What is it made from?
Speaker 2 (43:12):
Glucose.
It's made from starch.
Speaker 1 (43:13):
Does it have another name on the market?
Speaker 2 (43:15):
Allulose.
Well, there are companies thatsell it like RX sugar, but no,
the name isn't allulose, it'sthree beta hydroxy fructose,
whereas fructose is three alphahydroxy fructose.
So it's an epimer of fructose.
It's not as sweet as fructose,obviously, but it seems to have
some benefit.
Speaker 1 (43:33):
Whether that will hold up in long-term studies
(43:59):
whether it will actually lead toweight loss, whether it will
actually prevent leaky gut.
We don't know yet because thosestudies are not yet finished,
but at least from a big one.
But there seems to be a growingbelief that some of our
depression, anxiety, is tied towhat we eat.
Speaker 2 (44:08):
Yes.
Well, there's no question thatour depression and our food are
related to each other.
That I'm very confident in,100%.
The question, of course, isthrough what mechanism, and
there are possibly several, soit's not that simple.
One may have to do with themitochondrial dysfunction that
we talked about before.
(44:28):
One may have to do with changesin neurotransmitters in the
brain, like glutamate to GABA.
So glutamate's an excitatoryneurotransmitter, gaba is an
inhibitory neurotransmitter.
Gaba is an inhibitoryneurotransmitter, okay, and
sugar actually interferes withthat conversion.
Normally glutamate goes to GABA, but sugar actually prevents it
.
So you end up with increasedexcitatory, decreased inhibitory
(44:49):
, and that may cause problems.
In addition, insulin resistancecauses changes in some of the
trophic factors in the brain,such as leptin and BDNF, and
these are trophic factors thatcause neurite outgrowth and, in
some cases, increasedneurogenesis in certain parts of
the brain.
Then there's the microbiomestory, which is, I think, what
(45:12):
you're trying to get at, and sowhat might be happening with the
microbiome is that theseultra-processed foods are
actually altering microbialdiversity and also short-chain
fatty acid production.
And short-chain fatty acidshave effects on the brain.
They circulate in thebloodstream, go to the brain and
have anti-inflammatory effects.
(45:32):
There are immune cells in thebrain called microglia.
There are immune cells in thebrain called microglia and when
you are inflamed peripherallyand in the gut, that reaches the
brain.
That signal reaches the braineither through the blood or
possibly through the vagus nerve, up the vagus nerve to activate
(45:52):
those inflammatory cells, thosemicroglia, and they go from an
M2 lineage to an M1 lineage,which basically tells them we're
in eating mode and that mayactually be part of the
cognitive decline and has beenassociated with the onset of
Alzheimer's.
So there's a lot of concernabout what's going on with these
(46:14):
various foods and what thesedifferent mechanisms, either
blood-borne or possibly throughthe vagus nerve, might be doing
to the brain to fomentdepression, Alzheimer's,
possibly schizophrenia.
We also know that patients withbipolar disorder and depression
who start on a ketogenic dietget better.
(46:35):
So is it because of the changein the mitochondria?
Is it because of the change inthe cytokines?
Is it because of the change inthe gut inflammation?
Maybe all three?
We don't know yet.
Speaker 1 (46:47):
As I think about companies again trying to make
things that are good for us,better for us, improve what is
being made available.
What is the definition of food?
Speaker 2 (46:57):
So I know the definition of food, carolyn, do
you, because I looked it up.
So the dictionary definition offood, which I am very
comfortable with, I'm 110% inline with this definition
Substrate that contributes toeither growth or burning of an
organism.
That is food.
So let's take sugar.
Does sugar contribute toburning?
(47:20):
Well, if you think it's a bombcalorimeter, you'd say four
calories per gram contributes toburning.
Except we're not bombcalorimeters.
We burn in our mitochondria andfructose inhibits mitochondrial
ATP generation by inhibitingthree separate enzymes that are
involved in generating ATP.
(47:42):
Fructose inhibits burning, itdoes not contribute to it, it
inhibits it.
What about growth?
Turns out, fructose inhibitsgrowth.
My colleague, dr EfratMonsenigo-Ornan, who runs the
nutrition department in HebrewUniversity, jerusalem, who runs
the nutrition department inHebrew University, jerusalem,
actually looked at this questionand showed that in fact,
ultra-processed food, andspecifically sugar, inhibits
(48:04):
long bone growth, cancellousbone growth, skeletal bone
growth, trabecular bone growth,cortical bone growth, and in
addition, it also does that inhumans, not just in rats.
Okay, so there are studies ofsugar consumption and
suppression of height in othercountries.
So it's obviously notcontributing to growth.
(48:27):
And, by the way, hijack ofcells by, you know, cancer cells
.
You know they love fructose.
They love feeding the cancercell because the rest of the
body can't use it, but thecancer cell can.
So in essence, you're basicallyhijacking growth with cancer.
So it's not contributing toburning, it's not contributing
(48:51):
to normal growth, it's onlyhijacking growth in cancer cells
.
That doesn't sound like food tome, does it?
Speaker 1 (48:58):
So can we just look at 10 years In your perfect
world with a good dose ofrealism, so imperfectly perfect
world.
Where could we get, with thewill of the people behind you,
in 10 years?
Speaker 2 (49:11):
To me, the line in the sand that has to be crossed
is food subsidies.
As long as there are foodsubsidies, we cannot solve this
problem.
People ask me all the time ifyou had a magic wand and you
could do one thing that wouldstick, what would it be?
I would get rid of all foodsubsidies, and the reason is
because they distort the market.
(49:32):
The reason ultra processed foodis cheaper than real food is
because of food subsidies.
If we got rid of the foodsubsidies, then they wouldn't be
, and so there wouldn't be animpetus for the food industry to
rely on them and there wouldn'tbe an impetus for the public to
purchase them.
Speaker 1 (49:50):
Is this specific to corn?
Speaker 2 (49:52):
Corn, wheat, soy, sugar, all of them and you'd
have to get rid of all thesubsidies for this to work.
So this was actually looked atat UC Berkeley many years ago,
called the Gene EatingFoundation, and they asked the
question what would the price offood look like if we got rid of
all food subsidies?
And the answer is it wouldn'tchange, except for two items
which would go up corn and sugar.
(50:13):
And that's what we'd want to goup, because if you raise the
price then you reduce effectiveavailability.
So you get rid of lower thedose on two poisons.
So for me, the food subsidyissue has to be dealt with and
has to be dealt with first.
The problem with that is thatthat takes Congress.
Speaker 1 (50:33):
Or a president.
Speaker 2 (50:34):
Well, it takes something.
Speaker 1 (50:36):
And there's no will in Congress because of farmers,
because they're all paid off.
Speaker 2 (50:42):
They're all paid off by the food and the farm
industry.
Have you ever heard of ALECA-L-E-C, the American
Legislative Exchange Council?
They're a bill mill.
They basically write bills andhand them to congressmen to
introduce them.
Those bills are for theirbenefactors.
You know who's paying Alexbills and who are those the farm
industry, the food industry,the oil industry, you know, and
(51:06):
the opiate industry.
Speaker 1 (51:07):
I think you have said , though, that knowledge is
probably the first frontier inchange.
Maybe I'm misphrasing, but doyou see a big change in the
knowledge of the generalpopulation about food?
Speaker 2 (51:21):
74% of Americans are trying to reduce their sugar
consumption because of the workthat's come out over the last 10
years.
So mine and others.
That's good.
In addition, it used to be thatpeople thought a calorie was a
calorie and now they're thinkingsugar is particularly egregious
in terms of calories.
And I didn't generate thosedata.
Ific generated those data.
(51:42):
The International FoodInformation Council, the public
relations arm of the foodindustry, found that out.
It used to be 11% of peoplethought it was sugar and now 40%
of people think it's sugarthat's driving the obesity and
diabetes epidemics.
The public is catching on.
The public is now aware it'sone of the reasons that RFK was
(52:05):
able to create this Mahamovement, because people say
there's a problem with the food.
Yeah, I've been saying it for along time now, but people are
starting to say it.
The question is not does RFKhave the right diagnosis?
He does.
The question is does he havethe right prescription?
Speaker 1 (52:26):
Good point.
You asked a brilliant questionon the Huberman podcast, which
is what is the largestrestaurant chain in the US?
Speaker 2 (52:35):
It is our nation's public schools.
Largest restaurant chain in theUS, it is our nation's public
schools.
They're three times bigger thanSubway, McDonald's, Burger King
and Wendy's all combined it'striple the size.
And our kids are getting sickerand sicker.
So we have started a nonprofithere in California called Eat
Real and our job is to get realfood into K-12.
(52:56):
Now to do that, we have tochange the business model in
each school or each schooldistrict to basically make real
food the standard, to be able toactually buy food at scale,
manufacture them in acentralized facility instead of
(53:20):
in each school separately, whichis what used to happen years
ago.
But now, because there's nofootprint even for food
preparation, because it's allbeen taken away by the schools
to create new classrooms, youknow the food has to be made off
site.
But we can basically teachschool districts how to get real
(53:41):
food to their students, and wenow have the data.
We're actually writing up thepaper right now to show the
improvement in academic scoreswhen kids eat real food.
Speaker 1 (53:53):
Dr Robert Lustig, thank you for your tireless
efforts to educate us and I'velearned so much again today.
I always learn from you.
I hope that we do see more andmore change.
I hope people's sweet toothdeclines.
Speaker 2 (54:07):
Well, Carolyn, you're part of the change.
Speaker 1 (54:09):
Onward and forward.
I can't wait for your newproducts to come out of the
company you're working with.
Speaker 2 (54:15):
We're doing our best.
We have a new fiber that we'reworking on that we hope will
start being incorporated intoCPG products around the country
and around the world, which wethink will mitigate the
metabolic burden ofultra-processed food and
hopefully make things better.
Speaker 1 (54:31):
Thank you so much.
Look forward to doing thisagain.
Speaker 2 (54:34):
My pleasure, Carolyn.
Speaker 1 (54:37):
If you enjoyed this session, please do comment, rate
and follow us on Apple Podcasts, spotify or wherever you listen
, and please share this withyour friends and colleagues.
What is the largest restaurant chain in the US?
Speaker 2 (00:07):
It is our nation's public schools.
They're three times bigger thanSubway, mcdonald's, burger King
and Wendy's all combined.
It's triple the size.
And our kids are getting sickerand sicker.
Speaker 1 (00:19):
Hello friends, old and new, and welcome to Drinks
with Caroline.
I'm so happy you've joined mefor what I believe will be
another stimulating conversationwith an industry expert,
founder or otherwise fabulousperson in the consumer industry.
Dr Robert Lustig, welcome toDrinks with Caroline.
(00:40):
I'm so excited to be asking youquestions 11 years or so later,
given that I got the wonderfuljob of doing this at the Hong
Kong Forum when I worked forCLSA, and then we had a dinner
afterwards and I was just blownaway by all the facts that you
gave us about the impact ofsugar on our metabolisms.
And I'm no less blown away inlistening to Dr Andrew Huberman
(01:06):
and you discussing this towardsthe end of last year, and so I'm
just very grateful that you'veagreed to come onto my podcast
Drinks with Caroline.
We are now supposed to splitopen a drink.
Speaker 2 (01:16):
Well, I'm just going to ask you would you rather it
be a sparkling water, or wouldyou rather it be a scotch?
You choose.
Speaker 1 (01:22):
Well, I must admit, given it's still morning in LA,
I am drinking a coffee right now.
Well, how do you start your day, Robert?
Speaker 2 (01:29):
Black coffee only.
Speaker 1 (01:31):
Black only.
Well, I've got to wean myselfoff oat milk, but unfortunately
it has sugar in it and I'maddicted, so I think this is a
great starting point.
Dr Robert Lustig is an MD, aneuroendocrinologist, emeritus
professor of pediatrics at UCSFand a best-selling author, and
has appeared on many podcastsand other public forums to
(01:54):
discuss the impact of sugar onthe American diet.
I just have to say thateverything you've done the hard
work and heavy lifting overdecades now to try and raise
awareness that protein and fataren't bad and sugar is really
causing mitochondrial diseaseand all sorts of other issues
I'm in awe and I know that thattakes a lot of courage.
Speaker 2 (02:14):
The food industry.
Initially, for the first, Iwould say 15 years of my
advocacy had painted a target onmy back and did its ultimate to
discredit me and the notion.
And I think the reason isbecause sugar was their gravy
train.
Sugar is what brought them tothe feeding trough.
Sugar was what made the profitmargin of virtually every CPG
(02:37):
company go from 1% per year upto 5% per year.
And the reason is because sugaris addictive.
They did not want us to talkabout sugar being a
mitochondrial toxin, but thefact of the matter is it is.
The data has shown it andpeople are starting to
understand and incorporate thatconcept into their thinking.
Speaker 1 (02:57):
Could you just tell us a little bit about your
background in working withchildren and then your
observations that led you towhere you are today?
Speaker 2 (03:04):
Before I get started on that, I want to make one
thing clear to your audience,and that is it's not just sugar,
it's ultra-processed food.
In general, sugar is the2,000-pound gorilla, but there
are other issues withultra-processed food as well,
including the lack of fiber, thelack of omega-3s and also the
presence of emulsifiers.
(03:25):
All of these ultimatelycontribute to defective
metabolism and increasedinflammation, which are driving
all the chronic diseases that weknow of today.
Having said that, the easy one,the thing that's, you know,
sort of staring us in the facethat needs to be fixed and we
(03:45):
could fix it tomorrow if we hadthe political will is get rid of
the sugar.
So that's kind of where I startand where I finish.
That's kind of the alpha andthe omega of the story.
So how do I get started?
Look, I'm a pediatricneuroendocrinologist.
I'm interested in how the braincontrols hormones and how
hormones control the brain.
So I'm very interested inbehavior.
(04:08):
Well, obesity was kind of likethe final frontier of
endocrinology.
We didn't really understandobesity until we discovered this
hormone that goes from your fatcell to your brain, called
leptin.
So leptin was discovered in1994, so 30 years ago, and I was
, you know, right there, youknow well placed.
(04:31):
At the time of its discovery.
I actually worked atRockefeller University, which is
where leptin was discovered,and sort of knew all of the
protagonists in the leptindiscovery story, and so I was
very prepared and ready for itbecause I knew it was coming.
I had just moved to St JudeChildren's Research Hospital in
Memphis, tennessee.
So this is a pediatric cancerhospital, and at St Jude they
(04:55):
had a cadre of about 40 childrenwho had survived their brain
tumors only to become massivelyobese afterward, either due to
the tumor itself or the surgeryor the radiation.
So this form of obesity is wellknown in the literature.
It's been known since 1901.
It's called hypothalamicobesity because the hypothalamus
(05:18):
is the brain area that controlsenergy balance.
And clearly these children havea problem with their
hypothalamus and that's why theybecome obese.
And I now have 40 of them.
And what am I going to do forthem when they weigh 350 to 400
pounds?
What can I possibly help themwith?
(05:40):
Previously these kids had beenstudied by other investigators,
like, for instance, george Bray,who's the father of obesity
research in America, and headmitted eight of these with.
Previously these kids had beenstudied by other investigators,
like, for instance, george Bray,who's the father of obesity
research in America, and headmitted eight of these kids to
his research unit at Harbor UCLAMedical Center back in 1975.
And he locked them up and threwaway the key and he fed them
(06:00):
500 calories a day for a month.
What do you think their weightdid on 500 calories a day?
Plunged, it went up.
Wow, the kids are on starvationdiets and they're gaining weight
on starvation diets.
Are they breathing the caloriesin?
No, turns out, because of thehypothalamic damage.
(06:21):
Their brain thinks they'restarving and the reason is
because they can't see thishormone called leptin, because
those neurons are dead.
And when you can't see yourleptin, your brain thinks you're
starving.
And so what they did was theywent into energy conservation
mode, their sympathetic nervoussystem, which normally burns
(06:42):
energy, even at rest, even whileyou're sleeping, you still have
.
Even at rest, even while you'resleeping, you still have a body
temperature.
Even while you're sleeping,because your muscles are still
working, they're still turningover ATP.
Even while you're sleeping,even though you're not moving,
well, their temperatures are waylower because they're actually
trying to conserve energy.
So, even on 500 calories a day,they're still gaining weight
(07:05):
and, of course, they're hungrylike crazy.
And so I've got these kids, andwhat am I going to do for them?
So I knew from my endocrinetraining that there was a nerve
that led from the hypothalamusto the pancreas called the
dorsal motor nucleus of thevagus nerve.
People know about the vagusnerve called the dorsal motor
nucleus of the vagus nerve.
(07:26):
When people know about thevagus nerve, it's what gives you
butterflies in your stomach.
Maybe if we did something tosuppress their insulin release,
maybe they wouldn't gain theweight.
So there's a drug that'savailable that I knew about,
called octreotide, and normallyit's used to suppress growth
hormone, but it also suppressesinsulin, and so we decided to
(07:48):
repurpose it and see whether ornot we could help these kids.
And so we did a pilot trial witheight children with this very,
you know, worrisome disordercalled hypothalamic obesity.
And lo and behold, they startedlosing weight.
But something even moreremarkable occurred Not only did
they lose weight, they startedexercising spontaneously.
(08:09):
One kid became a competitiveswimmer.
Two kids started liftingweights at home.
One kid became the manager ofhis high school basketball team,
running around collecting allthe basketballs.
These are kids who sat on thecouch, ate Doritos and slept,
and now they're active and theparents are saying I've got my
kid back and the kid's sayingthis is the first time my head
hasn't been in the cloud sincethe tumor.
This is really remarkable.
The very first patient Itreated with octreotide, you
(08:31):
know, with this hypothalamicobesity.
I tell the mother look, I don'tknow what's going to happen.
This is your patient number one.
I need you to call me in oneweek and tell me what's going on
.
She calls me in five days,frantic screaming in the phone.
Speaker 1 (08:46):
Dr Lustig, something's happening.
Speaker 2 (08:49):
And I'm going.
Oh my God, oh my God, adverseevent, shut this study down, go
to jail.
I'm waiting for the other shoeto drop.
What happened?
What happened?
Well, normally we would go toTaco Bell and she would eat five
tacos and an encharito andshe'd still be hungry.
We just went to Taco Bell andshe ate two tacos and she was
(09:10):
full and she just vacuumed thehouse.
Wow, just vacuumed the house.
I mean, this was a kid who didnothing, okay, and she vacuumed
the house.
So something was going on.
And this was before she hadever had a chance to lose any
weight.
It was, you know, just fivedays.
Okay, this kid weighed 220pounds and she ended up losing
(09:33):
48 pounds on octreotype.
So this was very, veryinteresting.
And so we did the study again.
This time we did it as adouble-blind placebo control
trial, and it worked again.
And then we did the study again.
This time we did it as adouble-blind placebo-controlled
trial, and it worked again.
And then we asked the questioncould this be going on in normal
people that don't have braintumors, you know, obese people
(09:55):
without a lesion in theirhypothalamus?
About 20% of the normal obesepopulation of adults responded
to octreotide the same way thekids did, with a suppression of
insulin and an increase inactivity.
So what we learned from thatexperiment is that the two
(10:18):
behaviors that we associate withobesity gluttony and sloth are
actually mediated by thebiochemical changes coming from
the brain, that the behavior isactually due to the biochemistry
.
And this changed how Iapproached all of obesity and
really what got me on the map interms of obesity research.
Speaker 1 (10:41):
That's a real breakthrough and I can't even
imagine how exciting and, at thetime, mind blowing.
I think more and more people,and particularly younger people
and people who listen to theHuberman podcast there's a group
that absolutely buys this.
I wanted to ask you a littlebit about calories in and
calories out, the CICA, andthere is definitely a group of
(11:06):
people that still firmlybelieves it's how many calories
you consume.
Can we address that?
Speaker 2 (11:11):
All I can say is that calories in, calories out is a
belief system, because you can'treally determine whether the
calories are going in or goingout.
You don't know.
Okay, how are you going tofigure that out?
Speaker 1 (11:23):
Well, what about these aura rings and things that
measure the output?
Speaker 2 (11:27):
That doesn't tell you here's the issue.
The whole world thinks a calorieis a calorie.
Now, for your audience, what'sa calorie?
So a calorie is a unit of heat,it's a unit of physics.
It is how much energy does ittake to raise one gram of water?
One degree centigrade, that'swhat a calorie is.
Now, in 1902, wilbur Atwaterfigured out that fat had nine
(11:53):
calories per gram of fat andprotein had four calories per
gram of protein and carbohydratehad four calories per gram of
carbohydrate.
Therefore, fat was more energydense.
Therefore, fat is fattening.
Speaker 1 (12:11):
Oh, wow.
Speaker 2 (12:14):
Because if a calorie is a calorie, then that would be
true, that would work, exceptthat that's ignoring several
issues.
Number one except that that'signoring several issues.
Number one insulin is thedriver of weight gain, and we
know that because all you haveto do is look at a type one
diabetic and look how muchweight they lose, and then you
put them on insulin and look atall the weight they gain back.
(12:35):
Number one.
Number two we are not bombcalorimeters.
Okay, if you put, you know, fatin a bomb calorimeter, you get
nine calories per gram, but weare not bomb calorimeters.
Okay, if you put you know, fatin a bomb calorimeter, you get
nine calories per gram, but weare not bomb calorimeters.
We have these things in ourcells called mitochondria, and
mitochondria are not bombcalorimeters.
Mitochondria can bedysfunctional.
(12:58):
Mitochondria don't necessarilyturn energy into heat, they turn
it into ATP, and there arerules governing how that gets
manufactured.
So I'll give you four, you know, killers to the idea that a
(13:19):
calorie is a calorie.
Okay, let's start with fiber.
Okay, fiber.
You like almonds?
Speaker 1 (13:28):
I wish I did, I don't .
Speaker 2 (13:30):
Okay, well, I love almonds, so you just have to
deal with it.
Okay, you eat 160 calories inalmonds.
How many of those calories doyou absorb?
130.
You ate 160.
You absorbed 130.
Where'd the other 30 go?
(13:50):
They were chewed up by themicrobiome.
You didn't absorb them becausethe fiber in the almonds
prevented their absorption.
So, even though they passedyour lips, even though they
registered as a calorie eaten,if you didn't absorb it, you
didn't get it, and if yourmicrobiome did, your microbiome
might do something with that.
That might actually change yourbehavior, like generate short
(14:13):
chain fatty acids which mightactually be immunosuppressive
and anti-inflammatory and reduceyour food intake.
Speaker 1 (14:22):
Just a question on that.
Then If you drank almond milk,you would not see that happen,
because you wouldn't get thefiber.
Speaker 2 (14:28):
There's no fiber, right?
Almond milk has no fiber.
Basically, the fiber got thrownin the garbage.
Same thing when you juice afruit you throw the fiber in the
garbage.
Turns out the fiber is the goodpart of the fruit.
The juice is nature's way ofgetting you to eat your fiber.
Speaker 1 (14:45):
Robert, one of the things that stuck with me a
decade is when you explained thedifference between eating four
oranges and trying to drink thatmuch.
Well, sorry, drinking that muchorange juice was easy the juice
of four oranges.
Trying to eat four orangeswould make you feel sick.
Speaker 2 (15:07):
You will throw up Right.
Speaker 1 (15:09):
And that just demonstrated the fiber issue.
Speaker 2 (15:12):
Yes, exactly so.
If you only measured thecalories at your mouth, you
would think that there'ssomething wrong, but in fact if
you measure them at theintestine, then it makes much
more sense.
But then a calorie is not acalorie, because a calorie eaten
is not a calorie eaten becauseif it came with fiber, that
(15:33):
calorie wasn't for you, it wasfor your bacteria.
Problem number one.
Problem number two protein.
So protein, as you know, ismade up of amino acids and each
amino acid can be used as astructural building block to
create other proteins, or it canbe used for energy.
Now, as it turns out, if youuse an amino acid for energy,
(15:56):
the liver has to take the aminogroup off, so it becomes an
organic acid, and then thatorganic acid can be used for
energy.
Well, in order to take thatamino group off, it costs energy
.
You have to invest energy inorder to get energy out.
So the mean difference betweenwhat you can burn in a bomb
(16:21):
calorimeter versus what yourcells will do with it will be
different, because you had toinvest energy in your cells,
whereas you didn't have toinvest the energy in a bomb
calorimeter.
So a calorie is not a caloriebecause if it came from a
protein, it ain't going to addup.
Number three, fats.
(16:42):
So over here we have omega-3sheart healthy, anti-inflammatory
, anti-alzheimer's, save yourlife, single best thing you can
put in your body.
Over here we have trans fats,the devil incarnate, okay,
consumable poison.
They're both nine calories pergram.
One will save your life, onewill kill you, because a calorie
(17:03):
is not a calorie.
And finally, the big kahunafructose and glucose.
So glucose is the energy oflife.
Every cell on the planet burnsglucose for energy.
Glucose is so important that ifyou don't consume it, your body
makes it.
Fructose, on the other hand, iscompletely vestigial to all
(17:24):
human life.
There is absolutely nobiochemical reaction in any
vertebrate on this planet thatrequires fructose.
It is a holdover from our plantancestors.
When we split off, they wentwith fructose, we went with
glucose, and that's why they'replants and we're not the point
(17:44):
is that's a great line.
Okay, well, actually some humansare plants, let's be honest,
but no plant is a human.
The point is, fructose ismetabolized in the liver
completely differently frombeta-glucose.
And what fructose does is itdrives liver fat because it
poisons mitochondriaspecifically to generate the fat
(18:07):
.
And the reason is becausefructose was only available one
month a year.
It was called harvest time, andwhat came after harvest time?
Winter.
So the goal of harvest was tosnarf up all of this fructose as
much as you could and get itturned into fat so that you
could basically survive thewinter.
(18:29):
We call this phenomenon seasonalinsulin resistance, and
fructose is specifically amitochondrial toxin so that your
cells will turn away fromburning it to energy, to ATP,
and turn it toward generatingfat.
And that worked for us forhundreds of thousands of years
(18:53):
as an adaptive evolutionarymechanism.
But when fructose is available24-7, 365, like it is now, we
don't need that, but we've stillgot it and we're still turning
it into fat, and so it's liningour arteries, it's lining our
livers, it's causing insulinresistance and it's driving
chronic metabolic diseasebecause it is metabolized
(19:17):
differently from that of glucose, because a calorie is not a
calorie.
So in a bomb calorimeter, sure,but we are not bomb
calorimeters, and anybody whosays a calorie is a calorie is
obviously not listening and, tobe honest with you, that's most
people.
Speaker 1 (19:34):
So can we talk about addiction?
And you make a reallyinteresting point about the huge
, the tectonic shifts in theworld systems, particularly in
the US, I guess, over the last50 years or so.
And how do you think sugarcould play out?
Speaker 2 (19:51):
So the question is is sugar addictive?
Now let's look at alcohol,because alcohol and sugar are
very similar to each other.
Because, after all, where doyou get alcohol from
Fermentation of sugar?
They actually are metabolicallyequivalent and in the brain
they're equivalent as well.
40% of Americans areteetotalers never touch the
stuff.
40% are social drinkers.
(20:12):
Can pick up a beer, put it down, I'm in there.
10% are binge drinkers and 10%are chronic alcoholics.
So 20% of America have analcohol problem.
Now, what constitutes being analcoholic?
What constitutes being alcoholaddicted?
We don't know To this day.
We don't know.
(20:32):
We've been looking for thegenetics of alcoholism, haven't
found it.
We've been looking for thegenetics of smoking haven't
found it.
We don't know what leads oneperson to be addicted and
another person to not be.
But clearly some are and somearen't.
Well, the same thing for sugar.
Not everybody is addicted, butthose that are are.
(20:56):
And it's very easy to figureout who's who, because the
sugar-addicted person will tellyou oh, I have a horrible sweet
tooth.
That's sugar addiction, untilproven otherwise.
And the reason they'll tell youis because right now, that's
socially acceptable.
If, all of a sudden, sugaraddiction was not socially
acceptable, they wouldn't tellyou that, just like they won't
(21:17):
tell you they're an alcoholicand nowadays they won't even
tell you they're a smoker,because it's not socially
acceptable.
So I figure 20 to 25% ofAmerica is sugar addicted.
Okay, everyone likes it, butnot everyone needs it.
It's when you need it that'sthe problem.
(21:37):
Now, how do you know that it'saddictive?
Well, because it activates thesame reward mechanism as cocaine
, heroin, nicotine, alcohol,sugar, and it does the exact
same things.
And you can measure it in thebrain.
You can see it in the brain,you can measure it biochemically
, you can measure it with fMRI,you can measure it with PET
scanning.
It's doing the same thing andmore and more for less and less.
(22:03):
In other words, as the sugardose goes up, you end up with
less and less reward, the law ofdiminishing returns, also known
as tolerance, which is one halfof addiction.
The other half is eitherwithdrawal or dependence, and
sugar shows that as well.
So the bottom line is sugarmeets all the criteria for
(22:27):
addiction that cocaine, heroin,nicotine and alcohol do.
There's going to be a specialissue of the Frontiers in
Psychiatry all on food addictioncoming up later this year.
All about food addiction.
You know, when you actuallycome down to it.
There are only really two itemsin food that are truly
(22:50):
addictive, and they are sugarand caffeine.
Speaker 1 (22:54):
Is that why I'm enjoying my iced latte so much?
Speaker 2 (22:57):
You said it, I didn't .
Speaker 1 (22:58):
I'm going to be wearing a glucose monitor soon,
dr Lustig, and I'm wonderingwhat is going to happen when I
put that on and then drink this.
Speaker 2 (23:06):
You'll find out and that will help you understand
what your food is doing to yourmetabolic health, and it might
alter your choices.
And if you do, that will onlybe good.
So I am an advisor to a companyhere in the United States
called Levels Health, and whatwe do is we try to help people
(23:31):
understand what food does totheir metabolic health.
One of the tools at ourdisposal is the use of
continuous glucose monitors,because the higher the glucose
goes, the more insulin is goingto be released.
The more insulin is going to bereleased, the more weight
you're going to gain and theless well you're going to feel.
Glucose is a proxy for insulinand insulin is the driver of
(23:54):
weight gain.
So we have data to show thatpeople who use continuous
glucose monitors gain lessweight and, in many cases, lose
weight, and they also feelbetter, in part because they're
not having the highs and thelows, because those highs and
the lows make you eitherirritable or they make you
sleepy.
Speaker 1 (24:13):
That makes so much sense.
You've also developed youtalked about I think someone
else developed the NOVA system.
Can you talk a little bit aboutthat?
Speaker 2 (24:21):
Sure, I did not develop the NOVA system.
My colleague, dr Carlos Montero, who is a public health
epidemiologist at the Universityof Sao Paulo in Brazil, he
developed the NOVA system.
So what the NOVA system does isit categorizes food.
Instead of based on itsnutritional value, it
(24:43):
categorizes food based on itsdegree of processing.
There are four classes in NOVA.
So the easiest way to explainthis is with an example.
Let's take an apple.
Nova class one would be anapple picked off a tree.
Nova class two would be appleslices de-stemmed, de-seeded,
maybe de-skinned.
Nova class three would be applesauce, macerated, cooked,
(25:04):
possibly with a preservativeadded, maybe with extra sugar,
maybe not.
Nova class four would be aMcDonald's apple pie.
Now the question is how muchNova class 1 apple is in that
Nova Class 4 McDonald's applepie?
And the answer is onlyMcDonald's knows for sure.
But the question is are all ofthese different types of Nova
(25:28):
Class foods the same?
If you believe a calorie is acalorie, it shouldn't matter
where the calories came from.
So it shouldn't matter wherethe calories came from.
So it shouldn't matter if yourcalories came from, you know,
carrots or cheesecake orCoca-Cola or kumquats, because
if a calorie is a calorie, thenthey should all be equal.
(25:48):
Well, it turns out when youlook and Carlos did this when
you look at all the disease inthe data sets from all over the
world in terms of what peopleare eating, all the disease is
in that NOVA class four group.
None of it is in NOVA class onethrough three.
Speaker 1 (26:07):
How is that being measured?
When you say all the disease?
Speaker 2 (26:10):
The incidence of hypertension, the incidence of
diabetes, the incidence ofcardiovascular disease, the
incidence of cancer, theincidence of dementia, the
incidence of fatty liver disease, et cetera.
All of these chronic metabolicdiseases that are basically
killing people all over theworld and basically draining
healthcare dollars from everysingle developed and developing
(26:32):
country all over the world.
$11 trillion deficit per yearfor the care and treatment of
chronic metabolic disease, whichis more than the US or globally
.
That's globally.
Speaker 1 (26:44):
It's insane.
Speaker 2 (26:45):
But it's more than what the food industry is making
.
So that's not sustainable.
There's more money going outthan is coming in.
That's unsustainable.
And all of them aremitochondrial diseases and none
of them have treatments and allof them are driven by that.
Nova Class 4 ultra-processedfood category.
Speaker 1 (27:05):
It's interesting you say none of them have treatments
, because I guess GLP-1 drugsare not a treatment.
But what is your view of them?
Speaker 2 (27:13):
Okay, so how much time do we have?
Carolyn, glp-1s are complicatedand I'm going to be very honest
with you, I don't know theright answer to them.
I know a lot about them becauseI'm an endocrinologist.
I was there when the firstGLP-1 started being used, called
Xenotide, back in 2006.
And I've known about GLP-1 as amolecule as recently as 1987.
(27:36):
Okay, so it's been around for awhile, but NovoNordisk and
Lilly have done very big thingswith it.
I wear three hats I wear theclinician hat, I wear the
scientist hat and I wear thepublic health policy wonk slash
advocate hat, and how I feelabout GLP-1s depends on which
(27:57):
hat I'm wearing.
So when I'm wearing myclinician hat, I'm glad they're
here because they work.
I'm not saying they don't work.
They do work 16% weight lossfor semaglutide, 20% weight loss
for terzepatide.
They work.
And if you have morbid obesityand nothing else works, these do
, and that's a big deal.
(28:18):
So I'm glad they're here.
So, from a clinician standpoint, I'm very positive about them.
It just so happens most of thepeople who are taking it are not
people who need it, like, youknow, people in Hollywood.
That's a different problem.
That's an access problem, not aclinical problem.
Now let me put my scientist haton.
Why do they work?
Well, they work in two ways.
(28:41):
They work in two places.
The first place they work is onthe brain, and they work on
that reward center we talkedabout before to actually reduce
reward, so that basically, sugarin particular is not as
interesting, and so you cut downyour consumption of sugar,
ultra-processed food, et cetera,and that is good.
(29:01):
Now we had a drug available tous 20 years ago out of France,
from Sanofi, and the drug wascalled Ramanubant.
It was the anti-marijuana drug,it was an endocannabinoid
antagonist, it was theanti-munchies drug and it got
approved for obesity in Europe.
(29:22):
Never got approved in America,but in Europe it got approved.
And within two months of itsapproval and people starting to
use it, there were 21 suicidesand the drug got immediately
pulled.
And what we learned from thatlittle foray is rewards what
gets you up in the morning, andif you shut reward off, there's
(29:44):
no reason to live.
Well, glp-1 shuts off reward,and so GLP-1 agonists are
associated with an increasedincidence of depression.
We've been looking for suicideas a telltale sign of a problem.
So it's still on the market,but there's no question that
there is an increased risk ofdepression with the use of
(30:04):
GLP-1s because of its effects onthe brain.
But remember I said there weretwo places it worked.
The second place is on the GItract, specifically on the
stomach, and what it does is itreduces the rate of gastric
emptying.
It basically makes your GItract move slower and so you
(30:26):
don't want to eat because youstill got stuff in your stomach.
Right, so it's mechanical.
But what that does is it causesthe side effects the nausea,
the vomiting, the pancreatitisand, most recently, the
gastroparesis.
Gastroparesis stomach turns tostone.
3.9% of people who use GLP-1analogs get gastroparesis and,
(30:53):
of course, package insertdoesn't even say it.
So this is actually a lawsuitgoing on right now against the
GLP-1 companies forgastroparesis.
Speaker 1 (31:03):
Is it reversible or it just stays once you have it?
Speaker 2 (31:06):
So a lot of patients who have taken it and get
gastroparesis.
They go off it and thegastroparesis doesn't get better
.
So there's a big issue that's alittle bit concerning, don't
you think?
Speaker 1 (31:17):
It's a little terrifying, I think.
Speaker 2 (31:19):
And number three when you look at the weight loss,
when you look at what's actuallybeing lost, turns out to be
equal amounts of fat and muscle.
Losing fat is the good part,but losing muscle is not.
Losing muscle is a bad thing.
Ask any little old lady whobreaks her hip whether she
wishes she had a little bit moremuscle.
Losing muscle is associatedwith increased mortality,
(31:41):
sarcopenia, so losing muscle isnot such a good thing.
So what else causes you to losefat and muscle in equal amounts
?
Starvation, and why do youthink it's working?
It's because you're starving.
Okay, is that the best way tolose weight?
Starvation?
I don't think so.
Okay, it's been shown you know50 ways from Sunday that that's
(32:02):
not the best way to do this.
Okay, and only one third ofpeople who take GLP-1 analogs
actually lose any weight.
They only tell you about theresponders.
They don't tell you about theintent to treat model and
responders.
They don't tell you about theintent to treat model.
And so many people get sideeffects that they stop taking it
.
Or because it's so expensive,they stop taking it and all the
weight comes back plus some.
(32:23):
So what that's telling you isit's not actually fixing the
problem, it's just band-aidingthe problem, because the weight
all comes rushing back as soonas you stop it.
Okay, let me put my third hat on, my public health advocate hat.
All right, these drugs do work.
I'm not saying they don't, theydo.
All right, 16% weight loss forsemaglutide.
(32:47):
20% weight loss for zepatide.
True, okay, if everyone inAmerica who qualified for an
analog got it, that would be$2.1 trillion to the healthcare
system.
But the healthcare system is$4.1 trillion in expenses, so
that would be a 50% surchargeover what we're paying now.
(33:09):
We're paying now.
How are we going to afford a50% increase?
That's crazy, unless, of course, trump really means we're going
to reduce drug costs.
Ha ha, if you believe that Igot a bridge to sell you.
Conversely, and this is theimportant part, if we just got
added sugar consumption in thiscountry down to USDA guidelines
(33:32):
of 12 teaspoons per day, howmany grams in a teaspoon?
Four, so 12 would be 48 to 50.
Speaker 1 (33:40):
That doesn't sound so punitive, that sounds very
doable.
Well, it's not.
Speaker 2 (33:43):
That's the point.
It's not.
We're consuming 94 grams, Imean.
So basically it'd be cutting itin half.
If we just cut our sugarconsumption in half, we would
lose 29% weight loss.
We'd have 29% weight loss, sowe'd have better weight loss,
and instead of spending 2.1trillion, we would save 3.0
trillion.
So that's a $5.1 trillion swingwith better weight loss and no
(34:09):
side effects.
So which one makes more senseto you?
Speaker 1 (34:13):
Yep, you make some really, really interesting
points.
Can we talk a little bit?
I've seen the number that youthrew out that 73% of what's
sold in grocery stores has sugarin it or hidden sugars.
You know, I think theavailability of healthier food
is something most of thepopulation really does want now,
(34:36):
and I think if sugar is hiddenit makes it really hard to make
good choices.
Speaker 2 (34:42):
Indeed, indeed, and there are 262 names for sugar,
and the food industry uses allof them on purpose, because that
way they can hide it in plainsight, and that's one of the
reasons our consumption is at 94grams per day.
So we need fundamental reformof the entire food system.
(35:05):
I completely agree with that.
The question is will RFK beable to enact that?
Speaker 1 (35:14):
Does he want to do that.
Speaker 2 (35:16):
Well, he says he does , We'll see.
But I'm actually quiteconcerned because his initial
moves in this space do notportend confidence.
Speaker 1 (35:30):
Do you mean around the dyes, or do you mean his
views on vaccines?
Speaker 2 (35:33):
Both.
I'm holding my breath andbiting my tongue and waiting,
but the things that I see so farare not exciting me.
Like, for instance, he wants toget rid of food dyes.
So do I.
We don't need them.
I totally agree.
On the other hand, instead ofasking Congress to ban them,
(35:58):
hand.
Instead of asking Congress toban them, okay.
Or instead of getting HHS toyou know, exert an
administrative order to removethem, okay.
He's basically said to the foodindustry please stop.
And they haven't.
So what good is that?
Speaker 1 (36:14):
Right, so I now live in LA.
There's a lot of innovation.
There are a lot of companiesthat do want to put good
products on the shelves, and isit possible to have processed
food that isn't bad for you?
Speaker 2 (36:27):
Yes, it is.
So here's the issue Ourultra-processed food is killing
us.
Our ultra-processed food isdecidedly unhealthy.
I completely agree with that.
The question is canultra-processed food be?
Speaker 1 (36:46):
made healthy?
Speaker 2 (36:47):
That's a different question.
I've been working for the lastfive years with a company in the
Middle East.
It's called Kuwaiti DanishDairy Company, add, and they are
like the Nestle of the MiddleEast and they make all sorts of
bad stuff.
They make flavored milks, theymake frozen yogurts, they make
ice cream, they makeconfectionery, they make
(37:09):
biscuits, they make tomato sauce.
Okay, like you know, problemstuff.
In 2020, the CEO of KDD came tome and said look, we know we
have a problem.
Kuwait has an 18% diabetes rateand an 80% obesity rate.
Speaker 1 (37:27):
Did you say 80% obesity rate?
Speaker 2 (37:29):
An obesity rate, oh my gosh.
And we don't want to be part ofthe problem, we want to be part
of the solution.
Can you help us turn KDD into ametabolically healthy company?
And so I don't take any moneyfor this.
But I convened a group ofscientific advisors and we
basically stemmed the stern topto bottom, took all the stuff
down to the studs, basicallyevaluated every aspect of KDD's
(37:53):
operation in terms ofingredients that they buy from
suppliers, processing techniquesand their products, okay, and
we sent them for biochemicalanalysis to actually determine
what's in the stuff.
And in doing so, we came upwith a set of precepts to
basically help KDD move theirproducts from unhealthy to
(38:15):
healthy.
And there are three preceptsthat determine whether or not a
given food is healthy.
And here are the three Protectthe liver, feed the gut, support
the brain.
Any food that does all three ishealthy, ultra-processed or not
.
Any food that does none of thethree is poison, ultra-processed
or not.
So, yes, ultra-processed foodin America right now satisfies
(38:38):
none of those three.
But could it?
Well, it would meanre-engineering ultra-processed
food.
Well, that's what we did withKDD, and so over the last two
years, kdd has pulled orre-engineered 10% of their
entire portfolio.
Re-engineered 10% of theirentire portfolio 18 items out of
(39:01):
180 items to become to bemetabolically healthy.
And then we've tested those inpeople to determine their
metabolic responses either theirglucose and insulin responses
or their GI responses, et ceterato determine whether or not
these maneuvers actuallyconferred health instead of harm
to these products.
And they are now on the marketin Kuwait.
(39:23):
So we wrote this up inFrontiers in Nutrition in 2023,
and we offered it to the worldas a roadmap for other companies
that want to do the same thing.
And what I can tell you is we'vehad no takers, and the answer
is because, number one, they'reafraid.
Number two, sugar's their gravytrain.
(39:44):
And number three, while theywould like to do something, they
have to worry about their wallstreet quarterly reports and
their stockholders.
In addition, if they said tothe public you know all that
processed food, we've been, youknow, serving up for the last,
you know 70 years, it's reallynot've been, you know, serving
up for the last, you know 70years.
It's really not that good foryou because we're going to try
to make it better.
Okay.
What they do is they losemarket share, they lose
(40:06):
reputation and they generatelawsuits.
This is all because they'reafraid.
Speaker 1 (40:11):
Demands of a shareholder group versus what
most human beings actually dowant to do and get right, I
think.
Speaker 2 (40:18):
Well, you know, the food industry is filled with
good people who want to do theright thing.
The problem is, they work for afood company.
Speaker 1 (40:25):
Can we talk about non-nutritional sugars like
replacements for sugar?
What is your view on those?
Speaker 2 (40:32):
If you believe a calorie is a calorie, then they
should be good because they'reno calories.
No fructose should be better.
Right Turns out, the metabolicdetriment of artificial
sweeteners does not go throughcalories or fructose, it goes
through other things.
So the toxicity of one sugarbeverage equals the toxicity of
(40:54):
two diet beverages.
Now you say to me, how can thatbe?
No sugar, no fructose, nocalories?
Well, it turns out those dietsweeteners do other things.
Number one they still generatean insulin response which still
generates weight gain.
And so it's been shown thatthrough meta-analyses that diet
sweetener consumption does notactually cause weight loss,
(41:18):
whereas if they did work theyshould cause weight loss, but
they actually don't because theystill generate an insulin
response.
And the second thing is thatseveral of the diet sweeteners
not all of them, but several ofthem actually cause GI
perturbations that lead tochanges in the microbiome,
glucose intolerance, leaky gutand therefore chronic
(41:39):
inflammation and systemicinsulin resistance, driving
chronic metabolic disease.
So even though these compoundsare zero calorie, that doesn't
mean they have zero effect.
Speaker 1 (41:53):
Which are the better diet sweeteners here.
Speaker 2 (41:56):
So we've done a full study of that for KDD and so I'm
very prepared to discuss it.
The one that seems to hold themost promise of all of them is
this compound called allulose,and allulose is an epimer of
fructose.
It seems to lower LDL and raiseHDL, which seems to be a good
thing from a cardiovascularstandpoint.
It seems to be able to be usedsimilar to sugar in terms of its
(42:20):
bulking capacity and itshumectant capacity and its
hardening capacity, so that'sgood.
It is 70% as sweet as sugar, soit can be used as a sugar
extender probably better as asugar extender than as a sugar
replacement, but even so seemsto have some benefit in value.
(42:41):
The problem with allulose rightnow is that it's 12 times as
expensive as sugar, so that'skind of keeping it out of the
market, and also the EuropeanFood and Safety Administration
has not approved it yet, in partbecause the way to make it is
with GMO processes, whichthey're not happy with.
So there are some questions.
And also now there are two newways of making allulose, so that
(43:04):
should reduce the pricesignificantly to maybe two times
the cost of sugar.
Speaker 1 (43:09):
What is it made from?
Speaker 2 (43:12):
Glucose.
It's made from starch.
Speaker 1 (43:13):
Does it have another name on the market?
Speaker 2 (43:15):
Allulose.
Well, there are companies thatsell it like RX sugar, but no,
the name isn't allulose, it'sthree beta hydroxy fructose,
whereas fructose is three alphahydroxy fructose.
So it's an epimer of fructose.
It's not as sweet as fructose,obviously, but it seems to have
some benefit.
Speaker 1 (43:33):
Whether that will hold up in long-term studies
(43:59):
whether it will actually lead toweight loss, whether it will
actually prevent leaky gut.
We don't know yet because thosestudies are not yet finished,
but at least from a big one.
But there seems to be a growingbelief that some of our
depression, anxiety, is tied towhat we eat.
Speaker 2 (44:08):
Yes.
Well, there's no question thatour depression and our food are
related to each other.
That I'm very confident in,100%.
The question, of course, isthrough what mechanism, and
there are possibly several, soit's not that simple.
One may have to do with themitochondrial dysfunction that
we talked about before.
(44:28):
One may have to do with changesin neurotransmitters in the
brain, like glutamate to GABA.
So glutamate's an excitatoryneurotransmitter, gaba is an
inhibitory neurotransmitter.
Gaba is an inhibitoryneurotransmitter, okay, and
sugar actually interferes withthat conversion.
Normally glutamate goes to GABA, but sugar actually prevents it
.
So you end up with increasedexcitatory, decreased inhibitory
(44:49):
, and that may cause problems.
In addition, insulin resistancecauses changes in some of the
trophic factors in the brain,such as leptin and BDNF, and
these are trophic factors thatcause neurite outgrowth and, in
some cases, increasedneurogenesis in certain parts of
the brain.
Then there's the microbiomestory, which is, I think, what
(45:12):
you're trying to get at, and sowhat might be happening with the
microbiome is that theseultra-processed foods are
actually altering microbialdiversity and also short-chain
fatty acid production.
And short-chain fatty acidshave effects on the brain.
They circulate in thebloodstream, go to the brain and
have anti-inflammatory effects.
(45:32):
There are immune cells in thebrain called microglia.
There are immune cells in thebrain called microglia and when
you are inflamed peripherallyand in the gut, that reaches the
brain.
That signal reaches the braineither through the blood or
possibly through the vagus nerve, up the vagus nerve to activate
(45:52):
those inflammatory cells, thosemicroglia, and they go from an
M2 lineage to an M1 lineage,which basically tells them we're
in eating mode and that mayactually be part of the
cognitive decline and has beenassociated with the onset of
Alzheimer's.
So there's a lot of concernabout what's going on with these
(46:14):
various foods and what thesedifferent mechanisms, either
blood-borne or possibly throughthe vagus nerve, might be doing
to the brain to fomentdepression, Alzheimer's,
possibly schizophrenia.
We also know that patients withbipolar disorder and depression
who start on a ketogenic dietget better.
(46:35):
So is it because of the changein the mitochondria?
Is it because of the change inthe cytokines?
Is it because of the change inthe gut inflammation?
Maybe all three?
We don't know yet.
Speaker 1 (46:47):
As I think about companies again trying to make
things that are good for us,better for us, improve what is
being made available.
What is the definition of food?
Speaker 2 (46:57):
So I know the definition of food, carolyn, do
you, because I looked it up.
So the dictionary definition offood, which I am very
comfortable with, I'm 110% inline with this definition
Substrate that contributes toeither growth or burning of an
organism.
That is food.
So let's take sugar.
Does sugar contribute toburning?
(47:20):
Well, if you think it's a bombcalorimeter, you'd say four
calories per gram contributes toburning.
Except we're not bombcalorimeters.
We burn in our mitochondria andfructose inhibits mitochondrial
ATP generation by inhibitingthree separate enzymes that are
involved in generating ATP.
(47:42):
Fructose inhibits burning, itdoes not contribute to it, it
inhibits it.
What about growth?
Turns out, fructose inhibitsgrowth.
My colleague, dr EfratMonsenigo-Ornan, who runs the
nutrition department in HebrewUniversity, jerusalem, who runs
the nutrition department inHebrew University, jerusalem,
actually looked at this questionand showed that in fact,
ultra-processed food, andspecifically sugar, inhibits
(48:04):
long bone growth, cancellousbone growth, skeletal bone
growth, trabecular bone growth,cortical bone growth, and in
addition, it also does that inhumans, not just in rats.
Okay, so there are studies ofsugar consumption and
suppression of height in othercountries.
So it's obviously notcontributing to growth.
(48:27):
And, by the way, hijack ofcells by, you know, cancer cells
.
You know they love fructose.
They love feeding the cancercell because the rest of the
body can't use it, but thecancer cell can.
So in essence, you're basicallyhijacking growth with cancer.
So it's not contributing toburning, it's not contributing
(48:51):
to normal growth, it's onlyhijacking growth in cancer cells
.
That doesn't sound like food tome, does it?
Speaker 1 (48:58):
So can we just look at 10 years In your perfect
world with a good dose ofrealism, so imperfectly perfect
world.
Where could we get, with thewill of the people behind you,
in 10 years?
Speaker 2 (49:11):
To me, the line in the sand that has to be crossed
is food subsidies.
As long as there are foodsubsidies, we cannot solve this
problem.
People ask me all the time ifyou had a magic wand and you
could do one thing that wouldstick, what would it be?
I would get rid of all foodsubsidies, and the reason is
because they distort the market.
(49:32):
The reason ultra processed foodis cheaper than real food is
because of food subsidies.
If we got rid of the foodsubsidies, then they wouldn't be
, and so there wouldn't be animpetus for the food industry to
rely on them and there wouldn'tbe an impetus for the public to
purchase them.
Speaker 1 (49:50):
Is this specific to corn?
Speaker 2 (49:52):
Corn, wheat, soy, sugar, all of them and you'd
have to get rid of all thesubsidies for this to work.
So this was actually looked atat UC Berkeley many years ago,
called the Gene EatingFoundation, and they asked the
question what would the price offood look like if we got rid of
all food subsidies?
And the answer is it wouldn'tchange, except for two items
which would go up corn and sugar.
(50:13):
And that's what we'd want to goup, because if you raise the
price then you reduce effectiveavailability.
So you get rid of lower thedose on two poisons.
So for me, the food subsidyissue has to be dealt with and
has to be dealt with first.
The problem with that is thatthat takes Congress.
Speaker 1 (50:33):
Or a president.
Speaker 2 (50:34):
Well, it takes something.
Speaker 1 (50:36):
And there's no will in Congress because of farmers,
because they're all paid off.
Speaker 2 (50:42):
They're all paid off by the food and the farm
industry.
Have you ever heard of ALECA-L-E-C, the American
Legislative Exchange Council?
They're a bill mill.
They basically write bills andhand them to congressmen to
introduce them.
Those bills are for theirbenefactors.
You know who's paying Alexbills and who are those the farm
industry, the food industry,the oil industry, you know, and
(51:06):
the opiate industry.
Speaker 1 (51:07):
I think you have said , though, that knowledge is
probably the first frontier inchange.
Maybe I'm misphrasing, but doyou see a big change in the
knowledge of the generalpopulation about food?
Speaker 2 (51:21):
74% of Americans are trying to reduce their sugar
consumption because of the workthat's come out over the last 10
years.
So mine and others.
That's good.
In addition, it used to be thatpeople thought a calorie was a
calorie and now they're thinkingsugar is particularly egregious
in terms of calories.
And I didn't generate thosedata.
Ific generated those data.
(51:42):
The International FoodInformation Council, the public
relations arm of the foodindustry, found that out.
It used to be 11% of peoplethought it was sugar and now 40%
of people think it's sugarthat's driving the obesity and
diabetes epidemics.
The public is catching on.
The public is now aware it'sone of the reasons that RFK was
(52:05):
able to create this Mahamovement, because people say
there's a problem with the food.
Yeah, I've been saying it for along time now, but people are
starting to say it.
The question is not does RFKhave the right diagnosis?
He does.
The question is does he havethe right prescription?
Speaker 1 (52:26):
Good point.
You asked a brilliant questionon the Huberman podcast, which
is what is the largestrestaurant chain in the US?
Speaker 2 (52:35):
It is our nation's public schools.
Largest restaurant chain in theUS, it is our nation's public
schools.
They're three times bigger thanSubway, McDonald's, Burger King
and Wendy's all combined it'striple the size.
And our kids are getting sickerand sicker.
So we have started a nonprofithere in California called Eat
Real and our job is to get realfood into K-12.
(52:56):
Now to do that, we have tochange the business model in
each school or each schooldistrict to basically make real
food the standard, to be able toactually buy food at scale,
manufacture them in acentralized facility instead of
(53:20):
in each school separately, whichis what used to happen years
ago.
But now, because there's nofootprint even for food
preparation, because it's allbeen taken away by the schools
to create new classrooms, youknow the food has to be made off
site.
But we can basically teachschool districts how to get real
(53:41):
food to their students, and wenow have the data.
We're actually writing up thepaper right now to show the
improvement in academic scoreswhen kids eat real food.
Speaker 1 (53:53):
Dr Robert Lustig, thank you for your tireless
efforts to educate us and I'velearned so much again today.
I always learn from you.
I hope that we do see more andmore change.
I hope people's sweet toothdeclines.
Speaker 2 (54:07):
Well, Carolyn, you're part of the change.
Speaker 1 (54:09):
Onward and forward.
I can't wait for your newproducts to come out of the
company you're working with.
Speaker 2 (54:15):
We're doing our best.
We have a new fiber that we'reworking on that we hope will
start being incorporated intoCPG products around the country
and around the world, which wethink will mitigate the
metabolic burden ofultra-processed food and
hopefully make things better.
Speaker 1 (54:31):
Thank you so much.
Look forward to doing thisagain.
Speaker 2 (54:34):
My pleasure, Carolyn.
Speaker 1 (54:37):
If you enjoyed this session, please do comment, rate
and follow us on Apple Podcasts, spotify or wherever you listen
, and please share this withyour friends and colleagues.
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